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LINC01783 accelerated tongue squamous cell carcinoma progression via inhibiting miR‐199b‐5p
Growing studies illustrated that lncRNAs exert critical roles in development and occurrence of tumours including TSCC. In this research, we indicated that LINC01783 was up‐regulated in TSCC cells (SCC1, Cal27, UM1 and SCC4) when compared to NHOK cell. RT‐qPCR analysis indicated that LINC01783 was ov...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8419183/ https://www.ncbi.nlm.nih.gov/pubmed/34363308 http://dx.doi.org/10.1111/jcmm.16352 |
Sumario: | Growing studies illustrated that lncRNAs exert critical roles in development and occurrence of tumours including TSCC. In this research, we indicated that LINC01783 was up‐regulated in TSCC cells (SCC1, Cal27, UM1 and SCC4) when compared to NHOK cell. RT‐qPCR analysis indicated that LINC01783 was overexpressed in 22 TSCC cases (73.3%, 22/30) compared with no‐tumour specimens. LINC01783 level was up‐regulated in TSCC specimens when compared to no‐tumour specimens. Ectopic expression of LINC01783 promoted TSCC cell cycle and growth and EMT progression in both TSCC cell SCC1 and Cal27. Overexpression of LINC01783 sponged miR‐199b‐5p in TSCC cell and elevated expression of LINC01783 inhibited miR‐199b‐5p expression. Moreover, we illustrated that miR‐199b‐5p was down‐regulated in TSCC cells and specimen and LINC01783 level was up‐regulated in TSCC specimens when compared to no‐tumour specimens. Elevated expression of LINC01783 promoted TSCC cell growth, cycle and EMT progression by sponging miR‐199b‐5p. These data suggested that LINC01783 functioned as one oncogene and might be one treatment target for TSCC. |
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